Allodynia

p3: Haggenjos L Guesteditorial Less of my patient are left behind with their pain. p5: Spicher CJ, Fehlmann P, Maihöfner C, Sprumont P, Létourneau E, Dyer JO, Masse J, López-Solà M, Maupas E & Annoni JM Original article Management Algorithm of Spontaneous Neuropathic Pain and/or Touch-evoked Neuropathic Pain illustrated by prospective observations in clinical practice of 66 chronic Neuropathic Pain Patients. p33: Algoritmo para la gestión del dolor neuropático [Español]. p34: Algorithme de gestion des douleurs neuropathiques [Français]. p35: Algoritmo de gestão enciamento da dor neuropática [Português]. p37: Drezet N Lu pour vous Adhésion du patient [Français]. p39: Gardner E Aphorisme saisonier [Français, English, Deutsch].

Ce manuel est destiné aux rééducateurs, aux médecins généralistes et de toutes les spécialités, ainsi qu’aux patients qui cherchent désespé-rément une solution à leur douleur.

La méthode de rééducation sensitive diminue les douleurs neuropa-thiques depuis la peau partiellement engourdie ou hypersensible au tou-cher. La peau, qui est le plus grand organe du corps humain, est fréquemment soumise à des traumatismes qui provoquent de micro lésions nerveuses avec leur cortège de symptômes : des sensations de brûlures « comme un coup de soleil » ou « comme un feu à l’intérieur », des douleurs au caractère électrique « irradiations » ou « élancements », des fourmillements, par exemples. Cette méthode est basée sur la plasticité neuronale du systême neurologique somesthé-sique – des yeux de la peau vers le cerveau – qui permet de modifier la situation, même plus de vingt mois après la lésion.

Cette méthode, qui a 15 ans, est aujourd’hui encyclopédique et de re-nommée mondiale. Les thérapeutes qui la pratiquent dans 29 pays sont organisés en un Réseau de Rééducation Sensitive de la Douleur (RRSD) neuropain.ch, qui décerne le titre de Rééducatrice/teur Sensi-tive/tif de la Douleur Certifié(e) (RSDC®).

« Ce manuel va permettre de stimuler tous les professionnels de la santé qui se consacrent à la gestion de la douleur et aux problèmes qui y sont associés. »        Ronald Melzack, McGill University, Montréal.

Tout patient souffrant de douleurs neuropathiques aiguës ou chroniques et présentant une allodynie mécanique au niveau du membre supérieur, c’est-à-dire une « hypersensibilité » au toucher, peuvent bénéficier d’un traitement de rééducation sensitive, par la technique de contre stimulation vibrotactile à distance. La mise en place et la bonne évolution du traitement est dépendante non seulement de la sévérité de l’atteinte, mais aussi de facteurs personnels, environnementaux et des habitudes de vie propre à chaque patient. Et n’oublions pas l’importance de l’évaluation rigoureuse, et de l’ « éducation thérapeutique » donnée par le thérapeute.

"The present study aimed at investigating the time span it takes to remove a static mechanical allodynia (SMA) in humans
suffering from chronic peripheral neuropathic pain. Forty-three subjects were included in the study and, during
somatosensory rehabilitation, their SMA territory was precisely mapped. They then underwent distant vibrotactile counter
stimulation (DVCS) treatment. It was observed that, with DVCS, SMA disappeared in all cases, and was transformed into
an underlying hypoaesthesia. It was found that the ‘‘tenderness to touch’’ symptom (which is SMA) was located in the same
territory as the underlying hypoaesthesia, which was located on a part of the cutaneous territory of a partially damaged nerve.
These results demonstrate that treating patients suffering from neuropathic pain with DVCS revealed a skin territory of
denervation that was previously masked by SMA. Thus, SMA can be considered as a paradoxical painful hypoaesthesia.
Furthermore, mapping SMA is a valuable source of information for our understanding of abnormal sensory processing in
neuropathic pain patients. We conclude that the mapping of the zone of hypersensitivity on the skin in humans suffering from
chronic peripheral neuropathic pain improves diagnosis. The mapping of the zone of hypersensitivity is a tool to presume
which branch of the peripheral nerve is damaged. The location of the axonal lesions is at the periphery, while the mechanism
of pain sensitization is probably central and referred peripherally to the skin by a painful hypoaesthesia."

Study Design: Retrospective cohort study.
Introduction: Somatosensory rehabilitation is a standardized method of evaluation and conservative treatment of painful disorders of vibrotactile sensation, including the mechanical allodynia and burning pain of complex regional pain syndrome (CRPS).
Purpose of the Study: The purpose of this study was to examine the effectiveness of somatosensory rehabilitation for reducing allodynia in persons with CRPS of 1 upper limb in a retrospective consecutive cohort of patients.
Methods: An independent chart review of all client records (May 2004-August 2015) in the Somatosensory Rehabilitation Centre (Fribourg, Switzerland) identified 48 persons meeting the Budapest criteria for CRPS of 1 limb who had undergone assessment and treatment. Outcomes of interest were the French version of the McGill Pain Questionnaire (Questionnaire de la Douleur St-Antoine [QDSA]), total area of
allodynia as recorded by mapping the area of skin where a 15-g monofilament was perceived as painful, and the allodynia threshold (minimum pressure required to elicit pain within the allodynic territory).
Results: This cohort was primarily women (70%), with a mean age of 45 years (range: 18-74). Mean duration of burning pain was 31 months (range: 1 week-27.5 years), and baseline QDSA core was 48. The average primary area of allodynia was 66 cm2 (range: 2.6-320), and the most common allodynia threshold was 4.0 g. The average duration of treatment was 81 days. At cessation of treatment, the average QDSA score was 20 (effect size Cohen’s d ¼ 1.64). Allodynia completely resolved in 27 persons (56% of the total sample where only 58% completed treatment).
Discussion: This uncontrolled retrospective study suggests that somatosensory rehabilitation may be an effective treatment with a large effect size for reducing the allodynia and painful sensations associated with CRPS of the upper limb. More work is in progress to provide estimates of reliability and validity for the measurement tools for allodynia employed by this method.
Level of Evidence: 2c.

The third study evaluated the use of somatosensory rehabilitation to decrease allodynia in a retrospective cohort of patients with CRPS. These patients had CRPS as defined by the Budapest criteria and had static mechanical allodynia as defined by a painful response to stimulation using a monofilament (15g). The treatment in this study included: 1) vibrotactile counter-stimulation applied away from the painful region; 2) vibration; and 3) avoidance of stimuli that induce pain. Following treatment, allodynia was completely resolved in 56% of the initial sample and pain qualities were reduced in 48 patients. The somatosensory rehabilitation program used in this study showed a large effect size in this sample of patients with upper extremity CRPS and provides preliminary evidence to support this method of treatment for patients with CRPS.

La névralgie crurale est une affection clinique assez fréquente et handicapante. Il existe de nombreuses formes cliniques en raison des variations anatomiques des différentes branches cutanées des nerfs saphène et fémoral. La neuroplasticité du système somesthésique est aujourd’hui démontrée et permet de mieux comprendre les modalités de la rééducation sensitive. Les différentes étapes de la prise en charge des patients souffrant de cruralgie sont expliquées avec précision. Les différentes stratégies du traitement de la rééducation sensitive sont mentionnées. Les traitements médicamenteux des douleurs neuropathiques périphériques sont brièvement rappelés. Enfin, le résultat de la rééducation sensitive d’une cruralgie (NNT = 1,8) est documenté sur la base d’un travail prospectif comprenant le suivi de 59 patients.

Pain is a signal and the information coming from the patient is it’s analyse. Allodynia is the definition of the phenomenon where the stimulation is different from the one we thought we would provoke a pain at that level. To paraphrase Rimbaud (a famous French poet), « My pain is another » ! If the physiological phenomenon is better known, the treatment is still a hazardous road for the therapist.

Pain is more then the mere representation of the nociceptive signal. From the periphery to the brain, the nociceptive signal will be modulated at all the levels of the central nervous system. The perception of pain is the finality of a complex series of endogenous mechanisms that will either emphasize the signal (excitatory mechanisms) or reduce the signal (inhibitory mechanisms). A chronic pain condition can produce changes that will affect these mechanisms in different ways. It is then not surprising that two patients presenting apparently similar pain problems may respond quite differently to the same treatment, since the physiopathology behind the pain is totally different.
Changes in the activity of the nociceptive system from the periphery to the cortex can be responsible for the development and maintenance of a chronic pain condition. However, they will implicate several different mechanisms that will respond differently to a treatment. Recent scientific data using brain imaging are supporting a cortical reorganization of white and gray matter in patients suffering from chronic pain [2; 26; 28; 32]. These observations are extremely important since these changes are reversible following an adequate treatment, including rehabilitation [15; 27; 47]. Based on our new understanding of the neurophysiology of pain, we are in front of a change of paradigm in the treatment of chronic pain. We can no longer look at chronic pain as a persistent acute pain condition, since the mechanisms and response to treatment will be totally different.

In order to engage in reflective practice, it is important to acknowledge what made my experience unique. I have come to identify similarities between the Swiss and the French Canadian practices, but also identified some discrepancies, shared by both environments. Albeit most often hardly perceivable, they deserve attention because they contribute to inequities and injustices, as well as perpetuating oppressive practices within healthcare systems and societies. This is especially important in light of recent international events, namely anti-racism solidarity protests originating from North America. This paper does not claim to offer answers, but rather to elicit an individual and communal attempt to reflect on our own practice as healthcare professionals.

« I wish that these e-News for Somatosensory Rehabilitation will constitute a network of rehabilitation, of teaching, but also of research for all the people who are interested in somatosensory rehabilitation. » (Spicher, e-News for Somatosensory Rehabilitation 1(1) p. 1),

Beyond these numbers, I believe that the most important aspect is the establishement of a platform where debates can occur, where opinion can converge and diverge. We are far from the uniform mindset that goes with the consensus-driven environment typically found in scientific communities. In bioethics (Sève, 1994), it is more important to seek the largest common denominator than the tiniest commun divisor. By constantly focusing only on the area of agreement, a consensus gradually forms until it is attained. On the contrary, the largest common denominator, like this e-news, tries to include the various languages of neurosciences, medicine, rehabilitation and especially of the people. Admittedly, there are some rules we chose not to follow. However, we do offer a wellspring of ideas, and from inclusion have found agreement and growth.

It is generally agreed that cold allodynia is a consequence of impaired (Aδ-fibre-mediated) central inhibition of C-nociceptive inputs. However, it is also known that C polymodal nociceptors are not activated at innocuous low temperatures. Recently, we demonstrated the contribution of C-tactile fibres to tactile allodynia. In this study, we investigated whether this, or a related, C-fibre class contributes to cold allodynia. In 30 healthy and 3 chronic pain subjects, a series of normally innocuous localised thermal stimuli were applied to the skin overlying a painful tibialis anterior muscle (induced by infusion of hypertonic saline). The effects of thermal stimulation on muscle pain were observed before and after compression blockade of myelinated fibres. Furthermore, intradermal capsaicin, menthol and TTA-A2 were used for desensitisation of TRPV1, TRPM8, and T-type calcium (Cav3.2) channels, respectively. Before muscle pain, all thermal stimuli were reported as nonpainful regardless of whether myelinated fibres were conducting or not. During muscle pain, dynamic skin cooling (32°C → 20°C) evoked significant and reproducible increases in the overall pain intensity (allodynia). This increase was short lived and locked to the dynamic phase of cooling with pain levels returning to baseline during sustained cooling. Dynamic warming (32°C → 39°C) had no effect on pain levels. Cold allodynia persisted after nerve compression and TRPV1 and TRPM8 desensitisation but was abolished by localised Cav3.2 blockade. In clinical subjects, C-fibre-mediated allodynia was observed without the need for experimental pain-producing manipulations. In conclusion, cold allodynia represents a non-TRPV1- and non-TRPM8-dependent phenomenon, which is mediated by low-threshold Cav3.2-expressing C fibres.